Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy

Cancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the in...

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Main Authors: Magdalena Kluska, Agnieszka Wanda Piastowska-Ciesielska, Paulina Tokarz
Format: Article
Language:English
Published: MDPI AG 2023-07-01
Series:Current Issues in Molecular Biology
Subjects:
Online Access:https://www.mdpi.com/1467-3045/45/8/399
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author Magdalena Kluska
Agnieszka Wanda Piastowska-Ciesielska
Paulina Tokarz
author_facet Magdalena Kluska
Agnieszka Wanda Piastowska-Ciesielska
Paulina Tokarz
author_sort Magdalena Kluska
collection DOAJ
description Cancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the influence of G0- and G1-arrest has not been elucidated. To study the cell cycle arrest-mediated resistance, we used MCF-7 cells and generated three populations of cells: (1) cells arrested in the G0-like phase, (2) cells that resumed the cell cycle after the G0-like phase and (3) cells arrested in early G1 with a history of G0-like arrest. We observed that both the G0-like- and the G1-arrested cells acquired resistance to apoptosis induced by oxidative stress, accompanied by a decreased intracellular reactive oxygen species and DNA damage. This effect was associated with increased autophagy, likely facilitating their survival at DNA damage insult. The cell cycle reinitiation restored a sensitivity to oxidative stress typical for cells with a non-modulated cell cycle, with a concomitant decrease in autophagy. Our results support the need for further research on the resistance of G0- and G1-arrested cancer cells to DNA-damaging agents and present autophagy as a candidate for targeting in anticancer treatment.
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spelling doaj.art-ac7c4f0111984f6cac651bb5517acab02023-11-19T00:41:39ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452023-07-014586325633810.3390/cimb45080399Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of AutophagyMagdalena Kluska0Agnieszka Wanda Piastowska-Ciesielska1Paulina Tokarz2Department of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, PolandDepartment of Cell Cultures and Genomic Analysis, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, PolandDepartment of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, PolandCancer cells are characterised by uncontrolled cell proliferation; however, some of them can temporarily arrest their cell cycle at the G0 or G1 phase, which could contribute to tumour heterogeneity and drug resistance. The cell cycle status plays a critical role in chemosensitivity; however, the influence of G0- and G1-arrest has not been elucidated. To study the cell cycle arrest-mediated resistance, we used MCF-7 cells and generated three populations of cells: (1) cells arrested in the G0-like phase, (2) cells that resumed the cell cycle after the G0-like phase and (3) cells arrested in early G1 with a history of G0-like arrest. We observed that both the G0-like- and the G1-arrested cells acquired resistance to apoptosis induced by oxidative stress, accompanied by a decreased intracellular reactive oxygen species and DNA damage. This effect was associated with increased autophagy, likely facilitating their survival at DNA damage insult. The cell cycle reinitiation restored a sensitivity to oxidative stress typical for cells with a non-modulated cell cycle, with a concomitant decrease in autophagy. Our results support the need for further research on the resistance of G0- and G1-arrested cancer cells to DNA-damaging agents and present autophagy as a candidate for targeting in anticancer treatment.https://www.mdpi.com/1467-3045/45/8/399autophagybreast cancercell cycleDNA damage responseoestrogenoxidative stress
spellingShingle Magdalena Kluska
Agnieszka Wanda Piastowska-Ciesielska
Paulina Tokarz
Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
Current Issues in Molecular Biology
autophagy
breast cancer
cell cycle
DNA damage response
oestrogen
oxidative stress
title Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
title_full Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
title_fullStr Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
title_full_unstemmed Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
title_short Cell Cycle Status Influences Resistance to Apoptosis Induced by Oxidative Stress in Human Breast Cancer Cells, Which Is Accompanied by Modulation of Autophagy
title_sort cell cycle status influences resistance to apoptosis induced by oxidative stress in human breast cancer cells which is accompanied by modulation of autophagy
topic autophagy
breast cancer
cell cycle
DNA damage response
oestrogen
oxidative stress
url https://www.mdpi.com/1467-3045/45/8/399
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